PES1 promotes BET inhibitors resistance and cells proliferation through increasing c-Myc expression in pancreatic cancer

Jin, Xin; Fang, Rui; Fan, Ping; Zeng, Lipeng; Zhang, Bin; Lu, Xiaoming; Liu, Tao

doi:10.1186/s13046-019-1466-7

Cited by 39 publications

(51 citation statements)

References 64 publications

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“…The discovery of some promising molecular targets for the treatment of PDAC provided a new direction for the diagnosis and treatment of PDAC. For example, Jin et al reported that, PES1 might be a promoting factor of tumor growth and a PDAC prognosis associated protein [23]. Goehrig et al found that, βig-h3 stromal-derived protein is a main factor driving the immune paracrine interaction mechanism of PDAC, which might be novel target in PDAC treatment [24].…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Analysis of the Transcriptional Expressions and Prognostic Value of S100A Family in Pancreatic Ductal Adenocarcinoma

Wang

Jin

et al. 2021

Preprint

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Background Pancreatic ductal adenocarcinoma (PDAC) remains a treatment-refractory malignancy with poor prognosis. It is urgent to identify novel and valid biomarkers to predict the progress and prognosis of PDAC. The S100A family have been identified as being involved in cell proliferation, migration and differentiation progression of various cancer types. However, the expression patterns and prognostic values of S100As in PDAC remain to be analyzed. Methods We investigated the transcriptional expressions, methylation level and prognostic value of S100As in PDAC patients from the Oncomine, GEPIA2, Linkedomics, and cBioPortal databases. Real-time PCR was used to detect the expressions of S100A2/4/6/10/14/16 in four pancreatic cancer cell lines and pancreatic cancer tissues from PDAC patients undergoing surgery. To verify the results further, immunohistochemistry was used to measure the expression of S100A2/4/6/10/14/16 in 43 PDAC patients’ tissue samples. The drug relations of S100As were also analyzed by using Drugbank. Results The results suggested that, the expression levels of S100A2/4/6/10/14/16 were elevated to PDAC tissues than in normal pancreatic tissues, and the promoter methylation levels of S100A S100A2/4/6/10/14/16 in PDAC (n = 10) were lower compared with normal tissue (n = 184) (P < 0.05). In addition, their expressions were negatively correlated with PDAC patient survival. Conclusions Taken together, these results suggest that S100A2/4/6/10/14/16 might be served as prognostic biomarkers for survivals of PDAC patients.

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Section: Discussionmentioning

confidence: 99%

Comprehensive Analysis of the Transcriptional Expressions and Prognostic Value of S100A Family in Pancreatic Ductal Adenocarcinoma

Wang

Jin

et al. 2021

Preprint

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“…Additionally, DEAD-box RNA helicase 56 (DDX56) is involved in the assembly of the 60S large ribosomal subunit and has been associated with lymphatic invasion and distant metastasis in CRC [ 33 ]. Pescadillo ribosomal biogenesis factor 1 (PES1), which has been reported as an independent poor prognostic factor in pancreatic cancer patients [ 34 ], is essential for 60S ribosomal subunit maturation and pre-rRNA processing [ 35 ]. Therefore, we speculated that the regulation of ribosome biogenesis by GTPBP4 plays an essential role in various types of cancer.…”

Section: Discussionmentioning

confidence: 99%

Determining the Clinical Value and Critical Pathway of GTPBP4 in Lung Adenocarcinoma Using a Bioinformatics Strategy: A Study Based on Datasets from The Cancer Genome Atlas

Zhang

Wang

Mao

et al. 2020

BioMed Research International

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Lung cancer is the leading cause of cancer-related death worldwide, and the most common histologic subtype is lung adenocarcinoma (LUAD). Due to the significant mortality and morbidity rates among patients with LUAD, the identification of novel biomarkers to guide diagnosis, prognosis, and therapy is urgent. Guanosine triphosphate-binding protein 4 (GTPBP4) has been found to be associated with tumorigenesis in recent years, but the underlying molecular mechanism remains to be elucidated. In the present study, we demonstrate that GTPBP4 is significantly overexpressed in LUAD primary tumors. A total of 55 genes were identified as potential targets of GTPBP4. GO enrichment analysis identified the top 25 pathways among these target genes, among which, ribosome biogenesis was shown to be the most central. Each target gene demonstrated strong and complex interactions with other genes. Of the potential target genes, 12 abnormally expressed candidates were associated with survival probability and correlated with GTPBP4 expression. These findings suggest that GTPBP4 is associated with LUAD progression. Finally, we highlight the importance of the role of GTPBP4 in LUAD in vitro. GTPBP4 knockdown in LUAD cells inhibited proliferation and metastasis, promoted apoptosis, and enhanced sensitivity to TP. Overall, we conclude that GTPBP4 may be considered as a potential biomarker of LUAD.

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“…Various studies have shown that high mRNA expression of c-Myc has been associated with drug resistance in pancreatic cancer and HPV-negative neck squamous cell carcinoma cells (33,34). It has also been shown that downregulation of c-Myc mRNA expression using siRNA could improve the efficacy of DEX in treatment of ALL (35).…”

Section: Sal Overcomes Dex-resistance In the Cem-c1 Cells By Downregulating C-myc Protein And Mrna Expressionmentioning

confidence: 99%

Salidroside overcomes dexamethasone resistance in T‑acute lymphoblastic leukemia cells

et al. 2021

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The aim of the present study was to analyze whether the use of salidroside (SAL) could overcome dexamethasone (DEX) resistance in T-acute lymphocytic leukemia cells. The human T-ALL DEX-resistant cell line, CEM-C1 and the DEX-sensitive cell line, CEM-C7 were used in the current study. The proliferation inhibition rates in these cells, treated with SAL and DEX alone, and in combination were detected using a Cell Counting Kit-8 assay, while the morphological changes of the cells were observed using an inverted microscope. Reverse transcription-quantitative PCR was used to detect the mRNA expression levels of the c-Myc and LC3 genes, while flow cytometry was used to detect the cell cycle distribution and the rate of apoptosis. In addition, western blot analysis was used to detect the protein expression levels of c-Myc, BCL-2, Bax, cleaved PARP and LC3. and acridine orange staining was used to detect the changes in acidic autophagy vesicles. It was found that SAL could effectively inhibit cell proliferation and induce apoptosis in the CEM-C1 and CEM-C7 cells. In addition, SAL promoted the induction of autophagy. The protein expression levels of c-Myc in the CEM-C1 cells were significantly higher compared with that in the CEM-C7 cells. SAL downregulated the mRNA expression levels of the c-Myc gene and protein in a dose-dependent manner. This suggested that SAL could inhibit the proliferation of the CEM-C1 and CEM-C7 cells, induce apoptosis and autophagy and overcome DEX resistance in the CEM-C1 cells. The mechanism may be associated with the downregulation of c-Myc.

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PES1 promotes BET inhibitors resistance and cells proliferation through increasing c-Myc expression in pancreatic cancer

Cited by 39 publications

References 64 publications

Comprehensive Analysis of the Transcriptional Expressions and Prognostic Value of S100A Family in Pancreatic Ductal Adenocarcinoma

Comprehensive Analysis of the Transcriptional Expressions and Prognostic Value of S100A Family in Pancreatic Ductal Adenocarcinoma

Determining the Clinical Value and Critical Pathway of GTPBP4 in Lung Adenocarcinoma Using a Bioinformatics Strategy: A Study Based on Datasets from The Cancer Genome Atlas

Salidroside overcomes dexamethasone resistance in T‑acute lymphoblastic leukemia cells

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